Does Hyperparathyroidism Cause Hair Loss?

Hyperparathyroidism (HPT) is a condition defined by the overactivity of one or more of the four small parathyroid glands located in the neck near the thyroid gland. This overactivity results in the excessive production of parathyroid hormone, which ultimately disrupts the body’s delicate mineral balance. Many patients seeking a diagnosis or treatment for this disorder express concern about unexplained hair thinning or loss. This article explores the specific biological connection between hyperparathyroidism and changes in hair health, detailing the mechanisms and the potential for recovery.

The Role of Parathyroid Hormone and Calcium Regulation

The four parathyroid glands are pea-sized organs situated just behind the thyroid, and their sole purpose is to produce Parathyroid Hormone (PTH). PTH is the body’s primary regulator of calcium and phosphate levels in the bloodstream. When calcium levels drop, the glands respond by releasing PTH to restore balance.

PTH acts on three main areas to increase calcium levels: the bones, the kidneys, and the small intestine. It signals the skeleton to release stored calcium into the blood (bone resorption). In the kidneys, PTH increases calcium reabsorption and triggers Vitamin D activation, which enhances the absorption of dietary calcium from the small intestine.

In primary hyperparathyroidism, the glands become overactive, often due to a non-cancerous tumor called an adenoma, and produce too much PTH regardless of the body’s needs. This excess PTH causes a persistent state of hypercalcemia. This chronic metabolic imbalance is the underlying mechanism that can eventually lead to symptoms, including changes in hair.

How Hyperparathyroidism Impacts Hair Follicle Health

Chronic metabolic disturbance caused by HPT is known to impact the hair growth cycle. The resulting hair thinning is often diffuse across the scalp and is frequently categorized as Telogen Effluvium. This condition occurs when a significant physiological stressor forces a large number of growing hair follicles into the resting phase prematurely.

The high levels of calcium and PTH act as a systemic stressor that disrupts the normal cycling of the hair follicle. Hair growth proceeds in three main phases: anagen (growth), catagen (transition), and telogen (resting). Chronic hypercalcemia shortens the anagen phase, causing more hairs to enter the resting telogen phase, leading to noticeable shedding approximately three to six months later.

Hyperparathyroidism can also indirectly affect hair health through associated nutritional deficiencies. The PTH-driven process involves Vitamin D, and suboptimal Vitamin D status is common in HPT patients. Adequate Vitamin D is necessary for the proper functioning of hair follicles, and its deficiency can exacerbate hair thinning. The overall metabolic stress associated with a chronic endocrine disorder can further compound the issue, contributing to a generalized weakening of the hair structure.

Treatment of HPT and Hair Recovery Potential

Diagnosis of hyperparathyroidism involves blood tests that measure the levels of Parathyroid Hormone and calcium. If these results confirm high levels, additional testing may be used to locate the overactive gland. The definitive treatment for primary hyperparathyroidism is a surgical procedure called parathyroidectomy, which involves removing the problematic gland or glands.

For patients with mild disease who do not qualify for surgery, medications are available to help manage high calcium levels. The goal of treatment is to normalize the calcium and PTH levels, thereby removing the underlying metabolic stressor. Once hormonal balance is restored, the body can begin to reverse secondary effects, including hair loss.

The prognosis for hair recovery after successful treatment is generally positive. Since the hair cycle operates on a long timeline, patients typically begin to notice regrowth only after six to twelve months post-treatment. This reflects the time needed for hair follicles to exit the prolonged resting phase and re-enter the active growth phase once internal chemistry has stabilized.